Detailed Information on Publication Record
2009
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
CHEMANI, Chanez, Anne IMBERTY, Sophie DE BENTZMANN, Maud PIERRE, Michaela WIMMEROVÁ et. al.Basic information
Original name
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
Name in Czech
Uloha lektinu LecA a LecB v poskozeni plic vyvolanych Pseudomonas aeruginosa a efekt ligandu na bazi sacharidu
Name (in English)
Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands
Authors
CHEMANI, Chanez (250 France), Anne IMBERTY (250 France), Sophie DE BENTZMANN (250 France), Maud PIERRE (250 France), Michaela WIMMEROVÁ (203 Czech Republic, guarantor), Benoit P. GUERY (250 France) and Karine FAURE (250 France)
Edition
INFECTION AND IMMUNITY, The American Society for Microbiology, 2009, 0019-9567
Other information
Language
Czech
Type of outcome
Článek v odborném periodiku
Field of Study
10610 Biophysics
Country of publisher
Norway
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 4.205
RIV identification code
RIV/00216224:14310/09:00029451
Organization unit
Faculty of Science
UT WoS
000265279900037
Keywords in English
lectin; infection;preudomonas aeruginosa
Tags
International impact, Reviewed
Změněno: 24/8/2009 16:15, prof. RNDr. Michaela Wimmerová, Ph.D.
V originále
Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (a-methyl-galactoside and a-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa
In English
Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (a-methyl-galactoside and a-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa
Links
| GA303/09/1168, research and development project |
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| MSM0021622413, plan (intention) |
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